Term
|
Definition
| ulcers that extend deep into the muscluaris mucosa |
|
|
Term
HELICOBACTER PYLORI INFECTION
NSAID USE
stree-related mucosal damage
hyper-secretion of gastric acid (Zollinger-Ellison's Syndrome)
viral infections (CMV, herpes, TB)
hypercalcemia
radiation
chemotherapy (hepatic artery infusions) |
|
Definition
|
|
Term
cigarette smoking
psychological stress
dietary factors - ETOH |
|
Definition
| contributing factors to peptic ulcers |
|
|
Term
transmitted by fecal-oral route
same household member infected
crowded living conditions
unclean water
consumption of raw vegetables |
|
Definition
| risk factors for H. pylori infections |
|
|
Term
age > 60 yo
previous peptic ulcer
history of GI bleed
corticosteroid use
high-dose NSAIDs
multiple NSAIDs
anticoagulation |
|
Definition
| risk factors for NSAID-induced ulcers |
|
|
Term
imbalance between aggressive and protective factors
aggressive factors = gastric acid and pepsin
mucosal defense and repair = mucus and bicarbonate secretion, epithelial cell defense, mucosal blood flow |
|
Definition
| pathopysiology of peptic ulcer disease |
|
|
Term
gram negative bacteria
resides between mucus layer and epithelial cells
survives via urease production: urease produces ammonia which creates a buffered area around H. pylori so that it is not destroyed by stomach acid
pathogenic mechanisms
direct mucosal damage
host immune/inflammatory response alterations
increased acid secretion |
|
Definition
| pathophysiology of PUD caused by H. pylori |
|
|
Term
mechanisms of mucosal damage:
direct irritation of the gastric epithelium - initiated by acidic properties
inhibition of prostaglandins - COX1 (protection of GI tract, kidneys, platelets) and COX2 (pain, inflammation) |
|
Definition
| pathophysiology of PUD caused by NSAIDs |
|
|
Term
partially selective non-salicylates:
etodolac
nabumetone
sulindac
meloxicam
diclofenac
celecoxib
non-acetylated salicylates:
salsalate
trisalicylate
higher risk include:
non-selective non-salicylates - indomethacin, piroxicam, ibuprofen, naproxen, ketoprofen, ketorolac, flurbiprofen
acetylated salicylates - aspirin |
|
Definition
| NSAIDs with a lower ulcer risk |
|
|
Term
epigastric pain (dyspepsia)
nocturnal pain
intermittent symptoms
heartburn, belching, bloating
nausea, vomiting, anorexia
ALARMING SYMPTOMS:
weight loss
anemia
bloody vomit (hematemesis)
tarry stool (melena)
dysphagia |
|
Definition
| clinical presentation of PUD |
|
|
Term
GASTRIC ULCER:
food precipitates pain
antacids provide minimal relief
higher mortality
DUODENAL ULCER:
pain occurs 1-3 hours after meals
relieved by food or antacids
HS pain |
|
Definition
| clinical presentation of a gastric vs. duodenal ulcer |
|
|
Term
H. PYLORI INDUCED ULCERS:
site of damage - duodenum
symptoms - epigastric pain
ulcer depth - superficial
GI bleeding - less severe
NSAID INDUCED ULCERS:
site of damage - stomach
symptoms - often asymptomatic
ulcer depth - deep
GI bleeding - more severe |
|
Definition
| clinical symptoms of H. pylori vs. NSAID induced ulcers |
|
|
Term
invasive = endoscopic
indications: age > 45 or alarming symptoms
histology
rapid urease test detects ammonia (d/c AST x 1 week prior)
culture - 100% specific but not feasible (H. pylori cannot grow in culture) |
|
Definition
invasive diagnostic tools for PUD
indications and process |
|
|
Term
indications:
urea breath test:
for diagnosis and to confirm eradication
d/c antibiotics or AST 2 weeks before or 4 weeks after treatment
patient takes carbon-labeled urea, if H. pylori is present the urea will be digested and the patient will breath off labeled CO2
antibody detection:
IgG
for diagnosis
antibodies may still be around for up to 6 months, so not a good test for eradication
stool antigen:
for diagnosis and to confirm eradication
d/c antibiotics or AST 2 weeks before or 4 weeks after treatment |
|
Definition
| non-invasive diagnostic tools for PUD and indications |
|
|
Term
initial screening test of choice -> antibody detection
if endoscopy needed -> biopsy urease test
verify H. pylori eradication -> urea breath test or stool antigen
indications of eradication testing: history of ulcer complication, gastric-associated lymphoma, gastric cancer, recurrence of symptoms |
|
Definition
| H. pylori test of choice for initial screening and eradication |
|
|
Term
pain relief
ulcer healing
prevent recurrence
reduce ulcer-related complications
H. pylori positive:
eradication of H. pylori
cure the disease
NSAID-induced:
rapid healing of the ulcer |
|
Definition
| treatment goals of PUD therapy |
|
|
Term
eliminate or reduce:
psychological stress
smoking
use of non-selective NSAIDs
avoid foods and beverages that exacerbate symptoms |
|
Definition
| non-pharmacologic therapy for PUD |
|
|
Term
1st line therapy
treat for a minimum of 7 days
10-14 days of treatment preferred
Drug 1
PPI BID (omeprazole, lansoprazole, pantoprazole, esomeprazole, rabeprazole)
PLUS
Drug 2
Clarithromycin 500 mg BID
PLUS
Drug 3
Amoxicillin 1 g BID OR metronidazole 500 mg BID |
|
Definition
| PPI-based 3 drug regimen for the treatment of H. pylori associated ulcers |
|
|
Term
advantages: inexpensive
disadvantages: frequent ADRs, poor compliance
take with meals and at bedtime (except PPI)
treat for 14 days
Drug 1
PPI BID
Drug 2
Bismuth subsalicylate 525 mg QID
Drug 3
metronidazole 250-500 mg QID
Drug 4
tetracycline 500 mg QID OR amoxicillin 500 mg QID OR clarithromycin 250-500 mg QID |
|
Definition
| bismuth-based 4 drug regimen for the treatment of H. pylori associated ulcers |
|
|
Term
discontinue or lower dose of NSAIDs
test for H. pylori and treat if present
PPIs preferred, especially if continuing NSAIDs
misoprostol appears as effective as PPIs
H2RA or sucralfate:
ulcer healing and symptom relief in 6-8 weeks
PPI:
ulcer healing in 4 weeks
larger gastric ulcers may require higher doses and longer treatment (may take up to 8 weeks to heal) |
|
Definition
| treatment of NSAID-induced ulcers |
|
|
Term
symptoms or ulcers persist:
> 8 weeks: duodenal
> 12 weeks: gastric
refer to gastroenterologist |
|
Definition
| treatment failures of PUD therapy |
|
|
Term
use antibiotics not previously used during initial therapy
use bismuth containing regimen + PPI
treat for 14 days
address compliance |
|
Definition
| 2nd line treatment of H. pylori induced ulcers |
|
|
Term
high dose PPI
address compliance |
|
Definition
| 2nd line therapy for NSAID-induced ulcers |
|
|
Term
rationale for continuous antiulcer therapy:
long-term maintenance of ulcer healing
prevent complications
not necessary following H. pylori eradication
indications:
history of ulcer-related complications
failed H. pylori eradication treatment
heavy smoking
NSAID use |
|
Definition
| maintenance therapy indications for PUD |
|
|
Term
no risk factors:
use least GI-toxic non-selective agent at lowest effective dose
options if patient has risk factors:
PPI + NSAID - > 60 yo; concurrent ASA, coritcosteroid, or anticoagulant
COX2 inhibitor alone - > 65 yo without CV risk factors; concurrent steroids or warfarin
misoprostol QID plus NSAID |
|
Definition
| primary prevention of NSAID-induced ulcers |
|
|
Term
gastrin producing tumor:
gastric acid hypersecretion
recurrent peptic ulcers
when to consider ZES:
multiple or refractory ulcers
recurrent PUD + esophagitis
ulcer complications
treatment:
high dose PPI |
|
Definition
| Zollinger-Ellison's Syndrome |
|
|
Term
|
Definition
| superficial erosions commonly involving the mucosal layer of the stomach |
|
|
Term
physiological stress -> acid hypersecretion -> gastroduodenal reflux -> decreased bicarbonate, decreased mucus, increased pepsin -> acute stress ulcer
physiological stress -> vasoconstriction -> GASTRIC HYPOPERFUSION -> decreased PG synthesis, increased NO, increased ROS -> decreased mucus, increased inflammation and cell death -> acute stress ulcer
physiological stress -> vasoconstriction -> GASTRIC HYPOPERFUSION -> altered GI motility -> acute stress ulcer
physiological stress -> vasocontriction -> GASTRIC HYPOPERFUSION -> increased epithelial turnover, decreased bicarb, mucus, blood flow, and mucosal repair -> acute stress ulcer
GASTRIC HYPOPERFUSION IS THE PRIMARY ETIOLOGY OF STRESS ULCERS |
|
Definition
| pathophysiology of stress ulcers |
|
|
Term
| stress-related mucosal disease |
|
Definition
multiple asymptomatic lesions
unlikely to perforate
bleeding occurs from superficial mucosal capillaries |
|
|
Term
ICU patients
not recommended for non-ICU patients
reasonable to treat non-ICU patients with >/= 1 risk factor |
|
Definition
| indications for stress ulcer prophylaxis |
|
|
Term
MECHANICAL VENTILATION > 48 HOURS
COAGULOPATHY (PLT < 50,000 OR INR > 1.5)
acute renal failure
acute hepatic failure
severe head injury
thermal injury of > 35% BSA
major trauma
spinal cord injury
major surgery (lasting > 4 hours)
history of GI ulceration or bleeding within 1 year |
|
Definition
| major stress ulcer risk factors |
|
|
Term
ICU stay > 1 week
occult bleeding lasting >/= 6 days
high dose corticosteroids
sepsis |
|
Definition
minor stress ulcer risk factors
patients should have >/= 2 for prophylaxis |
|
|
Term
volume and hemodynamic support
enteral nutrition
pharmacologic therapy:
gastroprotective agents - sucralfate, antacids
gastric acid suppression - H2RA, PPI |
|
Definition
| therapy options for stress ulcers prophylaxis |
|
|
Term
PO/NG administration
frequent doses
ADRs - constipation/diarrhea, accumulation of cations in renal impairment
potential for drug interactions |
|
Definition
| limitations of gastroprotective agents (sucralfate, antacids) |
|
|
Term
H2RAs:
superior to sucralfate
if CrCl < 50 mL/min decrease dose by 50%
advantages: less expensive, few drug interactions (except cimetidine)
disadvantages: renally dosed, mental status changes, hematologic effects, BID dosing
PPIs:
non-inferior to H2RAs
advantages: no renal dosing, daily dosing |
|
Definition
| H2RAs vs. PPIs for stress ulcers prophylaxis |
|
|
Term
no absolute contraindication to short-term use of prophylaxis medications
potential complications:
side effects
dosage adjustments
polypharmacy
cost
inappropriate continuation of therapy after discharge
duplication of therapy
nursing time taken to administer drugs |
|
Definition
|
|
Term
higher gastric pH with AST leads to bacterial overgrowth
nosocomial penumonia
community acquired pneumonia
Clostridium difficile colitis |
|
Definition
|
|
Term
PUD: mostly NSAID related
stress ulcers
esophagitis
erosive disease
esophageal varices
Mallory-Weiss tear: longitudinal tear of the esophagus near the stomach; caused by excessive vomiting due to alcoholism, bulimia
neoplasm |
|
Definition
| causes of upper GI bleeds |
|
|
Term
hematemisis and/or melena
blood NG aspirate or lavage
coffee-ground emesis
severe cases indicated by hemodynamic changes: hypotension, hypoxia, decreased Hgb/Hct |
|
Definition
| clinical presentation of upper GI bleeds |
|
|
Term
> 75 yo
comorbidities
high transfusion requirements
shock/hypotension
hematemesis
red blood on rectal exam
continued bleeding or re-bleeding
blood in gastric aspirate |
|
Definition
| predictors of mortality with an upper GI bleed |
|
|
Term
age > 65 yo
comorbidities
high transfusion requirements
shock
coagulopathy
erratic mental status
red blood on rectal exam
hematemesis or melena
blood in gastric aspirate
Hgb < 10 or Hct < 30
endoscopic indicators:
active bleeding
visible vessel
adherent clot
ulcer location on posterior or superior wall
ulcer size > 2 cm |
|
Definition
| predictors of persistent upper GI bleed |
|
|
Term
hemodynamic support:
fluid resuscitation
packed red blood cells
vasopressors: to stabilize BP and HR
endoscopic evaluation and treatment:
hemostatic therapy - surgical coagulation during the endoscopy; heating mechanism to stop bleeding
sclerotherapy - medication (usually EPI) injected into the vessel to cause vasocontriction
more efficacious when combined with drug therapy
test for H. pylori
remove meds contributing to bleeding
PPI preferred adjuvant to prevent re-bleeding
use of PPIs decreases incidence of re-bleeding and need for surgery
risk for re-bleed greatest within 72 hours
HIGH DOSE PPI (HAVE TO KNOW DOSE!!)
omeprazole 80 mg bolus then 8 mg/h infusion x 72 h
or other PPI with equivalent dose
critically ill patients may not absorb oral medications
PO - only for low risk patients |
|
Definition
| treatment of an upper GI bleed |
|
|
Term
|
Definition
high risk therapy: ASA plus NSAID
what GI prophylaxis should be used? |
|
|
Term
|
Definition
high risk therapy: ASA or clopidogrel in high-risk patients (dual antiplatelets, history or GERD or PUD, >/= 60 yo, corticosteroid use)
what GI prophylaxis should be used? |
|
|
Term
|
Definition
high risk therapy: antiplatelet plus anticoagulant
what GI prophylaxis should be used? |
|
|
